Lipid emulsion to treat bupivacaine toxicity.
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Biomedical subjects
Publications and source records attributed to D Dalgleish.
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BACKGROUND AND STUDY AIMS: Patient-controlled sedation (PCS) using propofol and alfentanil provides effective sedation for colonoscopy, with the advantage of a shorter recovery time in comparison with diazepam and pethidine. However, most endoscopy units in the United Kingdom are currently using midazolam (a shorter-acting benzodiazepine) as a sedative agent. This study compares the efficacy of sedation and recovery times between PCS and a combination of midazolam and pethidine. PATIENTS AND METHODS: Sixty-seven patients undergoing colonoscopy were randomly assigned prospectively to receive sedation with either PCS, using propofol and alfentanil, or a bolus of midazolam and pethidine. Sedation and pain scores were recorded during the procedure by one specialist nurse. Patients' recollection of pain was recorded after the procedure. Recovery was assessed using number connection tests. The impact on subsequent activities and the level of amnesia, as well as overall satisfaction, were established by telephone call after 24 h. RESULTS: The sedation method had no impact on the success, difficulty, or duration of the colonoscopy. PCS could be set up by the specialist nurse without affecting the time between cases. Patients in the PCS group recovered significantly faster (median 5 min vs 35 min; P < 0.0001) and left the department more quickly (median 40 min vs 75 min; P < 0.0001). Patients in the PCS group had significantly higher pain scores and significantly more recall than those in the midazolam and pethidine group. All patients were satisfied with the sedation they received. CONCLUSIONS: PCS provides an acceptable alternative to sedation with midazolam and pethidine with the advantage of significantly faster recovery times, which are of relevance in the outpatient setting.
Recombinant protein kinase CK2 from the yeast Schizosaccharomyces pombe is able to phosphorylate casein in skimmed pasteurized milk. We could incorporate up to 540 pmol of phosphate into 50 microg milk proteins, i.e., 0.26 P/mol caseins. To better understand the action of protein kinase CK2 on milk proteins, we have compared the action of rspCK2alpha on milk, and on different casein micellar subfractions isolated from milk by ultracentrifugation. In contrast to the situation observed with phosphocaseinate, alpha(s) casein was the best substrate for rspCK2alpha, whether milk or micellar fractions were used as substrates. We have characterized the protein content of different micellar fractions obtained by ultracentrifugation of cow milk using capillary zone electrophoresis. We confirm that the kappa casein content of micelles largely decreases when their size increases. In contrast, the alpha(s) casein content slightly increased with micelles size and beta casein content remained constant. All of the micellar fractions were substrates for rspCK2alpha, but a significant amount of intrinsic protein kinase activity was also found. The intrinsic protein kinase used added ATP as phosphate donor, and was only slightly sensitive to high heparin concentration. It could phosphorylate micellar casein in milk ultrafiltrate, in the absence of addition of any metallic cofactor. Its activity was only slightly affected by the addition of either MgCl2 or MnCl2. CaCl2 activated the enzyme significantly. The intrinsic kinase lost its activity with time, and could incorporate from 9 to 26% of the total phosphate incorporated in the presence of rspCK2a. Alpha(s) casein was the best substrate of the intrinsic kinase, followed by beta casein. In the presence of CaCl2, the intrinsic kinase was found to incorporate up to 470 pmol of phosphate into 50 microg of milk proteins.
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Nine healthy volunteers were studied on the seventh day of dosing at 21:00 h with nizatidine 150 mg (N 150), nizatidine 300 mg (N 300), ranitidine 300 mg (R 300), or placebo, given in a predetermined random order. The double-blind 24 hour studies, using the Royal Free Hospital standard protocol, simultaneously measured intragastric acidity and plasma gastrin concentration. Compared with placebo, subjects responded to dosing with each H2-antagonist by a significant decrease of 24 hour intragastric acidity (N 150-45%; N 300-49% R 300-56%; p less than 0.01) and a significant rise of plasma gastrin concentration (N 150 + 20%; N 300 + 27%; R 300 + 58%; p less than 0.01). All three drug regimens caused similar significant decreases of nocturnal acidity (N 150-72%; N 300-79%; R 300-85%; p less than 0.01) and increases of nocturnal plasma gastrin concentration (N 150 + 41%; N300 + 52%; R 300 + 80%; p less than 0.01). Dosing with ranitidine 300 mg at 21:00 h also caused a simultaneous significant decrease of morning acidity (-32%; p less than 0.05) with a significant increase of plasma gastrin concentration (+36%; p less than 0.05), but the antisecretory effects of nizatidine 150 or 300 mg at 21:00 h were only observed during the night, with no effect during the morning. No drug regimen had any effect on acidity or plasma gastrin in the afternoon or early evening.
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